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首页> 外文期刊>Autoimmunity reviews >Potential role of human-specific genes, human-specific microRNAs and human-specific non-coding regulatory RNAs in the pathogenesis of Systemic Sclerosis and Sj?gren's Syndrome
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Potential role of human-specific genes, human-specific microRNAs and human-specific non-coding regulatory RNAs in the pathogenesis of Systemic Sclerosis and Sj?gren's Syndrome

机译：人类特异性基因，人类特异性microRNA和人类特异性非编码调控RNA在系统性硬化症和干燥综合征的发病机理中的潜在作用

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摘要

The etiology and pathogenesis of human autoimmune diseases remain unknown despite intensive investigations. Although remarkable progress has been accomplished through genome wide association studies in the identification of genetic factors that may predispose to their occurrence or modify their clinical presentation to date no specific gene abnormalities have been conclusively demonstrated to be responsible for these diseases. The completion of the human and chimpanzee genome sequencing has opened up novel opportunities to examine the possible contribution of human specific genes and other regulatory elements unique to the human genome, such as microRNAs and non-coding RNAs, towards the pathogenesis of a variety of human disorders. Thus, it is likely that these human specific genes and non-coding regulatory elements may be involved in the development or the pathogenesis of various disorders that do not occur in non-human primates including certain autoimmune diseases such as Systemic Sclerosis and Primary Sj?gren's Syndrome. Here, we discuss recent evidence supporting the notion that human specific genes or human specific microRNA and other non-coding RNA regulatory elements unique to the human genome may participate in the development or in the pathogenesis of Systemic Sclerosis and Primary Sj?gren's Syndrome.
机译：尽管进行了深入研究，人类自身免疫性疾病的病因和发病机制仍然未知。尽管迄今为止，通过全基因组关联研究已经取得了显着进展，但迄今为止，尚未明确证明特定基因异常是导致这些疾病的原因，这些遗传因素可能导致其发生或改变其临床表现。人类和黑猩猩基因组测序的完成为检验人类特异性基因和人类基因组独有的其他调控元件（如microRNA和非编码RNA）对多种人类发病机制的可能贡献开辟了新的机会。疾病。因此，这些人类特异性基因和非编码调控元件可能参与了非人类灵长类动物中不会发生的各种疾病的发展或发病机制，包括某些自身免疫性疾病，例如系统性硬化症和原发性干燥综合征。综合症。在这里，我们讨论了最近的证据，这些证据支持以下观念：人类基因组特有的人类特异性基因或人类特异性microRNA和其他非编码RNA调控元件可能参与系统性硬化症和原发性干燥综合征的发展或发病机制。

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